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Background: HBV-associated decompensated cirrhosis (HBV-DeCi) is attracting considerable attention due to disease acceleration and substantial mortality. Macrophages regulate the fibrotic process in DeCi. Soluble CD206 (sCD206) is primarily expressed by macrophages. We aimed to investigate whether sCD206 predicts mortality in patients with HBV-DeCi., Materials and Methods: A total of 382 patients were enrolled between February 2020 and February 2021 and divided into nonsurviving and surviving groups according to 28-day, 3-month, and 6-month outcomes. Cox regression analysis was performed to confirm the independent prognostic factors of HBV-DeCi, and Kaplan-Meier analysis was performed to draw survival curves of sCD206. The predictive value of sCD206 was assessed at three time points according to the AUROC., Results: The serum sCD206 level was significantly higher in deceased patients than surviving patients. Multivariate analysis showed that the level of sCD206 was related to an increased risk of 28-day, 3-month, and 6-month mortality (HR = 3.914, P < 0.001; HR = 3.895, P < 0.001; and HR = 4.063, P < 0.001, respectively). Patients with higher sCD206 levels had a worse prognosis than those with lower sCD206 levels. The best separation between the decedents and survivors was obtained by using the sCD206 level (AUROC: 0.830, 0.802, and 0.784, respectively) at 28 days, 3 months, and 6 months., Conclusion: The macrophage-related marker serum sCD206 was associated with mortality in HBV-DeCi patients. High levels of serum sCD206 indicated a poor prognosis in these patients. Serum sCD206 has great predictive value for short-term and midterm mortality compared with the Child-Turcotte-Pugh (CTP) and model for end-stage liver disease (MELD) scores., Competing Interests: The authors declare that there are no conflicts of interest., (Copyright © 2022 Yue Zhang et al.)

Background: Previous studies have reported that platelet count is associated with the progression of liver disease caused by hepatitis B virus (HBV), but there have been no reports on whether platelet count is associated with immune recovery in HIV/HBV co-infected patients., Methods: A retrospective analysis was conducted on 167 HIV-infected patients whose continuously highly active antiretroviral therapy (HAART) strategy was lamivudine +tenofovir+ efavirenz, of which 75 were HIV/HBV co-infected patients and 92 were HIV mono-infected patients. The biochemical examination results and demographic characteristics of all patients before HAART were collected, and routine blood test results (including platelet count) and immune cell count (including CD4 cells count) after all time points of HAART were obtained. All patients were observed until 72 months. CD4 cells count of 350 or 500 cells/μl 72 months after HAART served as the boundary for judging the immune reconstruction effect., Results: The basic characteristics of HIV/HBV co-infected patients and HIV mono-infected patients were matched. All patients had a good viral response (HIV RNA <20 copies/ml, HBV DNA < 100 copies/mL) and immune response during HAART. The platelets with poor immune recovery in HIV/HBV co-infected patients were also maintained at an apparent lower level than that in patients with good immune recovery. However, this phenomenon was not found in HIV mono-infected patients. The platelet level at many time points after HAART therapy in HIV/HBV co-infected patients can predict the effect of immune recovery at 72 months after HAART., Conclusion: The platelet counts of HIV/HBV co-infected patients were correlated with CD4 counts during the follow-up of HAART. These results suggest that the mechanisms associated with thrombocytopenia may be involved in the regulation of immune recovery after treatment in HIV/HBV co-infected patients., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2020. Published by Elsevier B.V.)

Current antiviral therapies against hepatitis B virus (HBV) infections, such as treatment with nucleos(t)ide analogs (NAs) and interferon alpha, can significantly lower HBV DNA titers, eventually to undetectable levels. However, it is still difficult to completely eliminate the stable template of HBV, the covalently closed circular DNA (cccDNA), and this contributes to viral rebound when treatment is discontinued. HBV pregenomic RNA (pgRNA), which was recently found to be present in the enveloped mature HBV viral particle in blood, is tentatively regarded, with still accumulating clinical evidence, as a novel bona fide virological marker reflecting the amount and status of cccDNA when serum HBV DNA becomes undetectable. HBV pgRNA and DNA share almost identical sequences, and it is therefore difficult to differentiate pgRNA from viral DNA using normal PCR methods. To exclude interference from viral DNA, methods for measuring pgRNA usually require a selective DNA degradation step, which is complicated and time-consuming and also compromises the accuracy of detection. In this study, we developed a simplified quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay with improved accuracy achieved by probing the polyA tail of pgRNA. Using clinical serum samples, we observed that not all patients share the same 3' sequence, suggesting slight differences between HBV strains in the way they end transcription. We then designed and evaluated a universal primer and probe set for distinguishing HBV pgRNA from HBV DNA. Our results demonstrated that a one-step qRT-PCR assay could selectively amplify HBV pgRNA from a mixture of HBV RNA and DNA, which is valuable for clinical applications.

Background: Combined HIV infection can accelerate HBV-induced liver disease. It is known that HBV Pre-S deletion is closely related to HBV-associated terminal liver disease in HBV mono-infection. Currently, data on HBV Pre-S quasispecies feature deletion in HIV/HBV co-infected patients are lacking. Methods: The characteristics and blood samples of patients with chronic HBV infection were collected and classified into an HIV/HBV co-infection group and an HBV mono-infection group according to HIV antibody results before treatment. HBV DNA in serum was extracted. The HBV Pre-S region was amplified by nested-PCR and was further T-A cloned. Using the standard sequence of the matched genotype HBV as a reference, BioEdit 7.0 software was employed for sequence alignment. Results: HBV Pre-S regions were successfully amplified from 147 patients, including 71 cases in the HIV/HBV co-infected group and 76 cases in the HBV mono-infected group. The proportion of the HIV/HBV co-infected group with Pre-S quasispecies deletion was lower than that of the HBV mono-infected group. By analyzing the frequency of Pre-S quasispecies in the two groups, the frequency of Pre-S quasispecies in HIV/HBV co-infected patients with Pre-S quasispecies was higher than HBV mono-infected patients. The frequency of Pre-S quasispecies deletion of the S protein promoter region in the HIV/HBV co-infected group was significantly higher than that in the HBV mono-infected group. Conclusion: High-frequency Pre-S quasispecies deletions are predominant in HIV/HBV co-infected patients; however, low-frequency Pre-S deletions are predominant in HBV mono-infected patients, providing a reference for the pathogenesis of the accelerated progression of liver disease in HIV/HBV co-infection. [ABSTRACT FROM AUTHOR]

A retrospective analysis was conducted on HIV-infected patients whose continuously HAART strategy was lamivudine +tenofovir+ efavirenz. Propensity matching for 35 HBeAg-positive/HIV co-infected patients, 35 HBeAg-negative/HIV co-infected patients, and 70 HIV mono-infected patients. Immune recovery (including CD4 cells count, CD4/CD8 ratio, CD4 count multiples and CD4/CD8 multiples) of HBeAg-negative/HIV co-infected group are continuously lower than HBeAg-positive/HIV co-infected group and HIV mono-infected group. The result indicated that the mechanisms associated with HBeAg-negative may be involved in the regulation of immune recovery after HAART. • HBeAg status before HAART is associated with immune recovery. HBeAg-negative status before HAART delays immune recovery in HIV/HBV co-infected patients. • A long-term observational study was performed. The antiviral therapy of all HIV-infected patients was lamivudine, tenofovir and efavirenz continuously. • 1:1:2 nearest neighbor propensity score matching was performed to control baseline confounding factors. [ABSTRACT FROM AUTHOR]